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The expression of inflammatory cytokines, TAM tyrosine kinase receptors and their ligands is upregulated in venous leg ulcer patients: a novel insight into chronic wound immunity
Author(s) -
Filkor Kata,
Németh Tibor,
Nagy István,
Kondorosi Éva,
Urbán Edit,
Kemény Lajos,
Szolnoky Győző
Publication year - 2016
Publication title -
international wound journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.867
H-Index - 63
eISSN - 1742-481X
pISSN - 1742-4801
DOI - 10.1111/iwj.12473
Subject(s) - medicine , mertk , gas6 , immune system , downregulation and upregulation , innate immune system , receptor , immunology , inflammation , tumor necrosis factor alpha , proinflammatory cytokine , peripheral blood mononuclear cell , venous leg ulcer , cytokine , receptor tyrosine kinase , gene , biology , surgery , biochemistry , in vitro
The systemic host defence mechanisms, especially innate immunity, in venous leg ulcer patients are poorly investigated. The aim of the current study was to measure Candida albicans killing activity and gene expressions of pro‐ and anti‐inflammatory cytokines and innate immune response regulators, TAM receptors and ligands of peripheral blood mononuclear cells separated from 69 venous leg ulcer patients and 42 control probands. Leg ulcer patients were stratified into responder and non‐responder groups on the basis of wound healing properties. No statistical differences were found in Candida killing among controls, responders and non‐responders. Circulating blood mononuclear cells of patients overexpress pro‐inflammatory ( IL ‐1α, TNF α, CXCL ‐8) and anti‐inflammatory ( IL ‐10) cytokines as well as TAM receptors (Tyro, Axl, MerTK ) and their ligands Gas6 and Protein S compared with those of control individuals. IL ‐1α is notably overexpressed in venous leg ulcer treatment non‐responders; in contrast, Axl gene expression is robustly stronger among responders. These markers may be considered as candidates for the prediction of treatment response among venous leg ulcer patients.

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